On the other hand, previous studies have observed RhoA regulation of YAP activation instead of its inactivation and that effect appears to be less dependent on force.[60, 61, 62, 63] For instance, various human disease models (e.g., diffuse gastric cancer, glioblastoma tumorigenicity, abnormal human trabecular meshwork) implicate the activation of YAP that is dependent on RhoA activation. Here, YAP1 is linked to glioblastoma.